The present disclosure relates generally to electric plasma synthesis of nitric oxide (NO) from gases and, more specifically, to systems and methods for a cooled NO generator to be used in medical applications.
NO is a crucial mediator of many biological systems, and is known to selectively regulate pulmonary arterial and systemic pressure, help the immune system kill invading parasites that enter cells, inhibit the division of cancer cells, transmit signals between brain cells, and contribute to the death of brain cells that debilitates people with strokes or heart attacks, among other things. NO mediates the relaxation of smooth muscle present, for example, in the walls of blood vessels, bronchi, the gastrointestinal tract, and urogenital tract. Administration of NO gas to the lung by inhalation has been shown to produce localized smooth muscle relaxation within the lung's blood vessels and is widely used to treat pulmonary hypertension, pneumonia, hypoxemic respiratory failure of a term newborn, etc. without producing systemic side effects such as systemic vasodilation and hypotension.
Inhaling NO can immediately produce potent and selective pulmonary vasodilation that improves the matching of ventilation with perfusion, thereby increasing an injured lung's oxygen transport efficiency, and breathing NO can raise the arterial oxygen tension. Breathing NO produces the rapid onset of pulmonary vasodilator action occurring within seconds of commencing breathing with the absence of systemic vasodilatation. Once inhaled, NO diffuses through the pulmonary vasculature into the bloodstream, where it is rapidly inactivated by combination with oxyhemoglobin (the NO dioxygenation reaction). Therefore, the vasodilatory effects of inhaled NO are limited to the lung in the treatment of acute and chronic pulmonary hypertension. Inhaled NO can also be used to prevent ischemia reperfusion injury after percutaneous coronary intervention in adults with heart attacks. Furthermore, inhaled NO can produce systemic anti-inflammatory and anti-platelet effects by increasing the levels of circulating NO biometabolites (including cyclic guanosine monophosphate) and by other mechanisms, such as the oxidation of circulating ferrous hemoglobin to ferric hemoglobin (methemoglobin) in the plasma. Further still, NO has known anti-microbial activity.